title: Postshock intervention with high-lipid enteral nutrition reduces inflammation and tissue damage.
abstract: OBJECTIVE
  To investigate the effects of high-lipid enteral nutrition in a setting of developing inflammation and tissue damage.
  
  
  BACKGROUND
  An excessive inflammatory response following severe trauma is associated with poor clinical outcome. Currently, therapies directed at attenuation of an ongoing inflammatory cascade are lacking. Administration of high-lipid enteral nutrition before hemorrhagic shock has been shown to effectively inhibit early and late proinflammatory cytokines by activation of the autonomic nervous system via cholecystokinin (CCK)-receptors.
  
  
  METHODS
  A rat model of hemorrhagic shock was used in which animals were either fasted or treated with high-lipid or control low-lipid enteral nutrition. CCK-receptor antagonists were administered before feeding. Tissues and plasma were collected to assess inflammation and intestinal integrity.
  
  
  RESULTS
  Administration of high-lipid enteral nutrition after shock reduced plasma interferon-gamma (IFN-gamma) significantly in comparison with those in low-lipid-treated and fasted animals (P < 0.01 and P < 0.001, respectively). Also, interleukin (IL)-10 levels in plasma were decreased in comparison with those in fasted animals (P < 0.001). Enterocyte damage, expressed as circulating ileal lipid-binding protein (ILBP), was prevented by early high-lipid nutrition in comparison with that in low-lipid-treated and fasted animals (P = 0.05 and P < 0.001, respectively). Furthermore, high-lipid feeding preserved intestinal integrity in comparison with that observed in low-lipid-treated and fasted animals, as assessed by bacterial translocation (BT) to distant organs (P < 0.05 and P < 0.001, respectively) and ileal permeability to horseradish peroxidase (HRP) (P = 0.05 and P < 0.001, respectively). The protective effects of high-lipid intervention were nullified by CCK-receptor antagonists (IFN-gamma; IL-10; BT; and HRP; P < 0.05).
  
  
  CONCLUSIONS
  High-lipid enteral nutrition given postshock reduces inflammation and preserves tissue integrity via a CCK-receptor-dependent mechanism. These findings implicate that intervention with high-lipid enteral nutrition following events such as severe trauma is a potential therapy to attenuate the developing inflammatory response.
authors.affiliation: Department of Surgery, Nutrition and Toxicology Research Institute Maastricht, Maastricht University Medical Center, Maastricht, the Netherlands.
authors.forename: Jacco-Juri
authors.initials: JJ
authors.lastname: de Haan
authors.forename: Tim
authors.initials: T
authors.lastname: Lubbers
authors.forename: M'hamed
authors.initials: M
authors.lastname: Hadfoune
authors.forename: Misha D
authors.initials: MD
authors.lastname: Luyer
authors.forename: Cornelis H
authors.initials: CH
authors.lastname: Dejong
authors.forename: Wim A
authors.initials: WA
authors.lastname: Buurman
authors.forename: Jan-Willem M
authors.initials: JW
authors.lastname: Greve
mesh_terms: D000818:Animals; D018988:Bacterial Translocation; D004041:Dietary Fats / Q000008:administration & dosage*; D004750:Enteral Nutrition / Q000379:methods*; D004847:Epithelial Cells / Q000473:pathology; D007082:Ileum / Q000166:cytology; D007150:Immunohistochemistry; D007249:Inflammation / Q000517:prevention & control*; D007371:Interferon-gamma / Q000097:blood; D016753:Interleukin-10 / Q000097:blood; D008297:Male; D009195:Peroxidase / Q000097:blood; D051381:Rats; D017207:Rats, Sprague-Dawley; D011949:Receptors, Cholecystokinin / Q000037:antagonists & inhibitors / Q000502:physiology; D012771:Shock, Hemorrhagic / Q000473:pathology*; D019108:Tight Junctions / Q000378:metabolism / Q000473:pathology
chemical_list: D004041:Dietary Fats; D011949:Receptors, Cholecystokinin; D016753:Interleukin-10; D007371:Interferon-gamma; D009195:Peroxidase